Some women bleed to death following childbirth. If the blood supply to the uterus can be controlled soon after birth, such deaths can be prevented. The blood supply to the uterus is predominantly from the right and left uterine arteries. In most women, the origin of each uterine artery is from the anterior division of the internal iliac artery. The uterine arteries reach the uterus traveling in the retroperitoneum and broad ligament and inserting into the uterus at the junction of the cervix of the uterus with the body of the uterus in a region of the uterus referred to as the “isthmus”. The right uterine artery meets the uterus along its right lateral border at about the “9:00 o'clock” position; the left, at about the “3:00 o'clock” position. As the uterine arteries approach the uterus, they are sufficiently close to the lateral vaginal fornix (typically about 12 cm) to be touched during a bimanual pelvic examination and their pulsations can frequently be felt manually in early pregnancy.
As pregnancy advances, the uterus changes shape, increasing in volume to accommodate the growing fetus and placenta. As a result, the uterine arteries move away from the uterine introitus. The uterine arteries are fixed in two locations: the first is where they exit the retroperitoneum and enter the broad ligament and the second is where they insert into the uterus. In between these two fixed points, the uterine arteries course back and forth in the broad ligament, in a plurality of undulations over a distance of several centimeters, the undulations are only loosely attached to the broad ligament, and are surrounded by delicate fatty tissue.
As the uterus increases in volume during pregnancy, it expands out of the pelvis into the abdomen. Because the uterine arteries are fixed to the uterus, they are pulled upwards along with the growing uterus. In the process, the undulations of the uterine arteries in the broad ligament straighten. However, with the expansion of the uterus into the abdomen as the pregnancy term lengthens, the uterine arteries can no longer be palpated during a bimanual pelvic examination because they are too far away from the vaginal introitus to be reached by an examiner's fingers (typically about 19 cm). From the beginning of pregnancy to just after delivery, the insertion of the uterine arteries into the uterus typically move about 7 cm away from the vaginal introitus.
Two major events occur at birth; a baby is born and a placenta separates from the uterus. Although the birth of a baby is an immense physiological, mechanical, psychological, and social experience—except for the rare birth canal laceration—it is an insignificant vascular event.
Separation of the placenta, however, is a monumental vascular event. The approximately 100 uteroplacenta arteries that supply the placenta are radial arteries transformed and enlarged by placental trophoblast cells to the shape of trumpets at their insertion into the placenta base. As a result of their unusual shape, they deliver blood to the placenta at low velocity and high pressure. At the time of delivery, cardiac output is 6-7 L/min with blood flow through the uterus at 0.5-1.0 L/min. When the placenta separates from the uterus, the uteroplacental arteries trumpet a large volume of blood directly into the uterine cavity. Left unchecked, every woman would bleed to death within minutes. However, the vast majority of women do not because, during the nine months leading up to delivery, clotting and fibrinolytic proteins, and their control systems, increase in concentration in mother's blood. Following placental separation from the uterine wall, blood flow is slowed in the uterus by persistent, regular myometrial contractions. With increased clotting proteins present and blood flow slowed by uterine contractions, myometrial arteries clot. Shortly thereafter, clot in the uterus lyses and myometrium is reperfused. However, clot is not lysed in uteroplacental arteries. They scar and are never used again. After clot forms throughout the body of the uterus, placental tissue dies and over weeks is sloughed into the uterine cavity.
Although uterine contractions following birth are generally sufficient to slow the velocity of blood flowing through the uterus to initiate blood clot formation throughout myometrium, in some women uterine contractions are inadequate. In the postpartum hemorrhage literature, a uterus that does not contract is considered to be “atonic” and the patient is said to be suffering from “atony.” Without a mechanism to slow or stop the flow of blood through the uterus, women with atony would bleed to death following childbirth.
Currently, there is a hierarchy of medical and surgical post partum interventions designed to slow the flow of blood through the uterus and help initiate uterine clot. Manual stimulation of the uterus (“uterine massage”) may start uterine contractions and increase uterine tone. If uterine massage is ineffective, usually oxytocin, a hormone that helps the uterus contract, may be delivered intravenously to stimulate the uterus to contract. If oxytocin fails, ergot alkaloids and prostaglandins frequently can be administered to chemically stimulate uterine contraction. However, these pharmaceutical agents produce side effects on the vasculature not just in the uterus but throughout the body. Consequently, they are contraindicated in patients with hypertension, hypotension, toxemia, and other disease states, the very women that need postpartum hemorrhage control.
If the medical post partum managements fail, surgical interventions follow. The simplest form of surgical intervention is packing the uterus with towels and the like in an attempt to compress the bleeding placental bed sinuses and arteries to initiate clotting. If the uterine packing fails, more complex surgery is performed. One surgical technique includes performing a laparotomy and then encircling the uterus with gross sutures and compressing the uterus by cinching the sutures tight.
Other types and configurations of gross sutures have been applied to the uterus during laparotomy to compress myometrium to try to arrest postpartum bleeding. In an attempt avoid compressing myometrium with gross sutures, it has been proposed to compress branches of the uterine arteries, themselves by blindly clamping two standard ring forceps to each lateral vaginal fornix in an effort to stop the hemorrhage. Though noninvasive, this method has no means for positively identifying whether or nor any artery has been compressed by the two sets of forceps. As a result, the method has not been adopted.
To slow the flow of blood in the uterine arteries in a variety of clinical situations, bilateral internal iliac artery ligation has been performed since the late nineteenth century. However, because vascular surgery is not generally taught in obstetric residencies, the technique is not widely practiced. However, some have ligated the internal iliac arteries to slow blood flow to the uterus to treat postpartum hemorrhage. Though effective, these techniques are not universally available and there is considerable time delay between the onset of postpartum hemorrhage and the transfer to an angiographic suite—commonly in different parts of the same hospital. Furthermore, since angiography is performed by radiologists and babies are delivered by obstetricians, communication gaps arise between the two specialties. Though at times effective, the internal iliac arteries supply the whole pelvis, not just the uterus. Their occlusion, therefore, stops blood flow to more than just the uterus. Furthermore, because of complex external iliac artery to internal iliac artery anastomoses, occlusion of the internal iliac artery only lowers pressure in the uterine arteries, it does not completely stop flow in the uterine arteries. Recognizing these limitations, open, transperitoneal surgical ligation of the uterine arteries, and laparoscopic uterine artery occlusion have been developed to treat postpartum hemorrhage.
Ligation of the uterine arteries is effective at stopping postpartum hemorrhage, but the procedure is invasive and time consuming. Uterine artery occlusion is generally performed emergently, when loss of time may equate with loss of life. To reduce the operative time and the surgical skill requirements that accompany selective ligation of the uterine arteries, bilateral arterial “bulk” ligation has been performed on the ascending branch of the uterine artery. In a bulk ligation the area of the ascending uterine artery is bundled together with adjacent myometrium and ligated. A bulk ligation requires a surgical laparotomy.
Angiographic catheter-based occlusive methods directed by fluoroscopy have been developed to treat postpartum hemorrhage by stopping blood flow in the arteries that feed the uterus. However, because the angiographic methods are performed by different specialists at different locations, there is frequently insufficient time to perform them for effective treatment of PPH.
Frequently, as in the past, many surgeons today stop postpartum hemorrhage by performing a hysterectomy which is a major operation with significant morbidity and mortality. Moreover, the procedure leaves the mother infertile.
Accordingly, there is need for uncomplicated instruments that can be rapidly deployed to partially or completely terminate blood flow in blood vessels such as the uterine arteries, particularly in the case of PPH.